Arabidopsis R1R2R3-Myb proteins are essential for inhibiting cell division in response to DNA damage

被引：60

作者：

Chen, Poyu ^{[1
]}

Takatsuka, Hirotomo ^{[1
]}

Takahashi, Naoki ^{[1
]}

Kurata, Rie ^{[1
]}

Fukao, Yoichiro ^{[2
]}

Kobayashi, Kosuke ^{[3
]}

Ito, Masaki ^{[3
,4
]}

Umeda, Masaaki ^{[1
,5
]}

机构：

[1] Nara Inst Sci & Technol, Grad Sch Biol Sci, Takayama 8916-5, Ikoma, Nara 6300192, Japan

[2] Ritsumeikan Univ, Dept Bioinformat, Kusatsu, Shiga 5258577, Japan

[3] Nagoya Univ, Grad Sch Bioagr Sci, Chikusa Ku, Nagoya, Aichi 4648601, Japan

[4] JST, CREST, Chikusa Ku, Nagoya, Aichi 4648601, Japan

[5] JST, CREST, Takayama 8916-5, Ikoma, Nara 6300192, Japan

来源：

NATURE COMMUNICATIONS | 2017年 / 8卷

关键词：

CYCLIN-DEPENDENT KINASE; THALIANA; PLANTS; ATM; TRANSCRIPTION; MYB; PHOSPHORYLATION; DEGRADATION; ACTIVATION; CHECKPOINT;

D O I：

10.1038/s41467-017-00676-4

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Inhibition of cell division is an active response to DNA damage that enables cells to maintain genome integrity. However, how DNA damage arrests the plant cell cycle is largely unknown. Here, we show that the repressor-type R1R2R3-Myb transcription factors (Rep-MYBs), which suppress G2/M-specific genes, are required to inhibit cell division in response to DNA damage. Knockout mutants are resistant to agents that cause DNA double-strand breaks and replication stress. Cyclin-dependent kinases (CDKs) can phosphorylate Rep-MYBs in vitro and are involved in their proteasomal degradation. DNA damage reduces CDK activities and causes accumulation of Rep-MYBs and cytological changes consistent with cell cycle arrest. Our results suggest that CDK suppressors such as CDK inhibitors are not sufficient to arrest the cell cycle in response to DNA damage but that Rep-MYB-dependent repression of G2/M-specific genes is crucial, indicating an essential function for Rep-MYBs in the DNA damage response.

引用

页数：12

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